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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Nov 15, 2013

 

Mouse femur with an enchondroma-like structure.

Image by Lick Lai







WHO Child Growth Charts

 

 

 

A protein that keeps people — and their skeletons — organized

Most people think that their planners or their iPhones keep them organized, when proteins such as liver kinase b1 (Lkb1) actually have a lot more to do with it.

New research from postdoctoral fellow Lick Lai in the lab of University of Southern California (USC) scientist Andy McMahon published in Proceedings of the National Academy of Sciences (PNAS) sheds light on how this important protein keeps people organized on a basic level by promoting orderly skeletal growth and preventing skeletal tumors.


In a developing embryo, many bones form based on cartilage templates.

The study found that to form these templates, Lkb1 protein controls the progression of immature, dividing cartilage cells into larger, mature and fully differentiated cartilage cells.

Without Lkb1, the population of immature cartilage cells disproportionately increases, leading to skeletal tumors.


The way that Lkb1 controls the differentiation of cartilage cells is by suppressing what’s known as the “mammalian target of rapamycin (mTOR) pathway” — a very important complex of molecules that coordinates growth in response to available nutrients and other factors. Problems with the mTOR pathway have been implicated in a host of human diseases, including diabetes, obesity, depression and many cancers.


The influence of abnormal Lkb1 isn’t restricted to the skeleton, however. Mutant forms of Lkb1 are frequently present in patients with lung, cervical, breast, intestinal, testicular, pancreatic and skin cancers, and in patients with the Peutz–Jeghers syndrome, characterized by benign polyps in the gastrointestinal tract.


“By understanding Lkb1 and the mechanisms that control normal skeletal development, we also learn how we might prevent this development from going awry in cancers and other disorders,” said McMahon, who directs the USC Stem Cell initiative and the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC.

Abstract
Liver kinase b1 (Lkb1) protein kinase activity regulates cell growth and cell polarity. Here, we show Lkb1 is essential for maintaining a balance between mitotic and postmitotic cell fates in development of the mammalian skeleton. In this process, Lkb1 activity controls the progression of mitotic chondrocytes to a mature, postmitotic hypertrophic fate. Loss of this Lkb1-dependent switch leads to a dramatic expansion of immature chondrocytes and formation of enchondroma-like tumors. Pathway analysis points to a mammalian target of rapamycin complex 1-dependent mechanism that can be partially suppressed by rapamycin treatment. These findings highlight a critical requirement for integration of mammalian target of rapamycin activity into developmental decision-making during mammalian skeletogenesis.

Significance
The transition from a mitotic to a postmitotic, hypertrophic chondrocyte is a key regulatory event in the growing vertebrate skeleton. By using genetic approaches, cell culture, and cell transplantation models, we provide compelling evidence that attenuating the energy-sensing mammalian target of rapamycin complex 1 (mTORC1) pathway is critical for switching chondrocyte states. A failure of mTORC1 suppression in Lkb1 mutants leads to a dramatic disruption of the skeletal growth plate and the formation of cartilage tumors comprising undifferentiated chondrocytes that display differential sensitivity to two key cartilage growth regulators, Indian hedgehog and Igf. The study highlights the interconnection between energy sensing pathways, normal growth control, and tumorigenesis in the skeletal program.

Co-authors Brendan N. Lilley and Joshua R. Sanes from Harvard University also contributed to the paper.

National Institutes of Health/ National Institute of Diabetes and Digestive and Kidney Diseases Grant P01 DK056246 provided funding for the work in the McMahon lab, and Dr. Lai is a recipient of an Arthritis Foundation Postdoctoral fellowship.

Original press release: http://www.uphs.upenn.edu/news/News_Releases/2013/11/bale/